How To Reverse Alzheimers & Cognitive Decline with Pioneering Neuroscientist Dr. Dale Bredesen

Hello, lovely listeners, and welcome to the Longevity and Lifestyle Podcast, where I invite pioneers and thought leaders in all things longevity and lifestyle to give us the strategies, tools and practices to live better and help us reach our highest potential. Today's guest is Dr. Dale Bredesen, Chief Science Officer at Apollo Health and a prodigious innovator in medicine with over 30 patents to his name. His 30-plus years of medical research have put Dr. Bredesen at the forefront of research into Alzheimer's disease, prevention, and memory loss reversal. His research and discoveries have changed our understanding of the fundamental nature of Alzheimer's disease and led to revolutionary treatments. An internationally recognized expert in the mechanisms of neurodegenerative diseases, Dr. Dale Bredesen's career has been guided by a simple idea: that Alzheimer's as we know it is not just preventable, but reversible. Thanks to a dedicated pursuit of finding the science that makes this a reality, this idea has placed Dr. Bredesen at the vanguard of neurological research and led to discoveries that today underlie the protocol to reverse Alzheimer's disease and cognitive decline at any age. Dr. Bredesen earned his MD, medical degree, from Duke University Medical Center and served as chief resident in neurology at the University of California, San Francisco, UCSF, before joining Nobel laureate Stanley Prusiner's laboratory at UCSF as an NIH postdoctoral fellow. He held faculty positions at UCSF, UCLA, and the University of California, San Diego. Dr. Bredesen also directed the program on aging at the Burnham Institute before joining the Buck Institute in 1998 as founding president and CEO. In this episode, we dig deep into understanding why cognitive decline, Alzheimer's, and other neurodegenerative diseases should be treated with a 21st century approach, namely through investigating and solving for the cause of the disease, as well as his groundbreaking protocol for reversing cognitive decline at any age, medicine for longevity, and much more. Please enjoy. Thanks for listening.

Dale, it is an honor and pleasure to welcome you today on the Longevity and Lifestyle Podcast. I was introduced only a few months ago by chance to your book, The End of Alzheimer's Program: The First Protocol to Enhance Cognition and Reverse Decline at Any Age. And I'm truly grateful for the work you and your team have been doing as a pioneer in the field of reversing cognitive decline and Alzheimer's, and particularly because it is a very personal topic for me. My mother is suffering from memory loss, as well as several parents of friends of mine. And thanks to your book, The End of Alzheimer's Program, which I will link in the show notes, has raised awareness. And I've discovered that I have a single copy of the APOE4 gene, which my understanding is that I have a 30% lifetime chance of developing Alzheimer's if I do nothing proactively about solving it. But I'd love to start with that you have some exciting news about some trial results have just come back. Maybe you can talk a little bit about that.

Yes, thanks very much, Claudia von Boeselager. So we've just finished the first clinical trial in history in which instead of predetermining a pro-Crustacean prescription for a treatment where you just say, we're going to treat you blindly, and this is which what has been done with every clinical trial in the past. So you decide we're going to use this drug or we're going to use that drug or we're going to use, you know, this lifestyle change, what have you. That doesn't necessarily have anything to do with what is causing the problem. So, in our trial, we flipped the script, and the idea is you want to look at every single person and ask, what are all the contributors to your cognitive decline? And what we find is that typically there are several. It's not typically one. There are several things that are all contributing. No surprise, this is a complex chronic illness, Alzheimer's and pre-Alzheimer's. So, you look at all the different things for each person, and then you target those the things that are actually driving the decline with a precision medicine type of approach, which has worked very well, as you know, with oncology, but really hasn't been applied to cognitive decline successfully. And we're still writing these up for publication, so I can't give too many details, but what I can say is we had unprecedented improvements and not simply a slowing of the decline as we've heard with a number of drugs, but these are actually sustained improvements. So we're very excited about that. And really what it's telling us What the data are telling us is that Alzheimer's disease is now becoming optional. You don't have to— this is not an ineluctable problem for people who are— if you're not going to wait until you're in late stage in a nursing home, which gives you many years. This is a disease that, as you know, comes on for about 20 years between the beginning of the pathophysiology and the diagnosis of Alzheimer's disease, and that's been well described by serial cerebrospinal fluid studies, and PET scan studies. So you can really see this problem coming. And now, of course, there are new blood tests available as well. So the bottom line here is that if everyone gets on either prevention or early reversal, virtually no one need to be concerned about this. That's a fundamental change for a major global problem. As you indicated, this is a very common problem. About 15% of the population will die. In the United States, this is now the third leading cause of death. And as you indicated, it's one of the important genes. The most common important one is ApoE, and ApoE has, of course, 2, 3, and 4 are the different alleles. And so as an example, I'm a 3, 3, which is the most common. That's kind of vanilla. If you have zero copies of ApoE4, as you indicated, it's a lower risk, and that's about 9% for your life. If you have a single copy, as you mentioned, it's a 30% lifetime risk, and that's 75 million Americans have a single copy. The vast majority do not know. It's about 25% of the population. And the reality is, if you do the appropriate prevention or early reversal, you should be able to reduce your risk to virtually zero, very, very close to zero. And then if you have 2 copies, and that's about 7 million Americans, it's about 2% of the population, then your risk is between 50 and 90%. Depending on other genetics. And so it's more likely that you will get Alzheimer's than that you will avoid it. And again, doing the right things, you can make sure that that is virtually zero. And there's a wonderful website started by Julie Gee, who is a 4/4 herself, who's gone from 35th percentile on her cognitive scores to 98th percentile. Wow. Really doing very, very well and actually was one of the co-authors. Of the End of Alzheimer's program because she is a citizen scientist and she's using this herself each day. So really tremendously complementary to my own background and skillset, along with my wife, Dr. Aida Lashin-Bredesen, who is a tremendous clinician and integrative physician. So we have a scientist, we have a clinician, and we have a daily user, which I thought was a really good way to get all the facts and all the helpful tips and hints and workarounds to the people who need them. So this is really a new era with cognition.

So exciting and such pioneering work that you're doing. And you mentioned just briefly that she's working on a website, or she has a website. What is that website?

Yes, good point. It's called apoe4.info. So if you check that out, it's wonderful. There are over 3,000 people who are ApoE4 positive from all around the world who share information. The vast majority of them are on some version of the protocol that we developed.

Excellent. So you mentioned the importance of knowing your APOE4 status. What tests would you recommend, and also what other types of tests would you recommend in general would be essential for anybody to know that might not be tested?

That's a great point. And so the testing that you want is actually rather extensive because human organisms are complex. Your brain is a complex organ, so you want to know the various things that contribute to it. When we started looking into what drives this, and we spent 30 years in the lab looking at what actually drives the phenomenon of neurodegeneration, what are the genes, what are the proteins, what's the biochemistry, what are the underlying mechanisms? What we found was that you could actually see the changes essentially as a balance. You have a whole set of biochemistry, a whole set of things, molecules, your genetics, your exposures, all these things that are causing your brain to be able to support itself. Literally what we call synaptoblastic signaling. You're making and keeping synapses. And on the other hand, there's a whole set of things that are on the other side of that. Things like inflammation, things like various pathogens and toxins and poor vascular support and mitochondrial damage and things like that. That are now telling your brain you're going to have to downsize, and that's synaptoclastic signaling. So literally, your probability of developing Alzheimer's is proportional to your ratio over time of synaptoclastic signaling over synaptoblastic signaling. So when we evaluate people, we want to understand what are the things that are driving the potential synaptoclastic signaling. What are the things— this is, by the way, no different than what you would do with osteoporosis, where you You have osteoblasts that are making bone and osteoclasts that are taking up the bone. Same idea here. This is literally like synaptoporosis. So we are looking at those things, and they break down into basically the subtypes that we described of Alzheimer's. So you want to know if there's ongoing inflammation. Simple tests you can do like hs-CRP to determine whether you have ongoing inflammation, and even simple things like albumin to globulin ratio. There are other ones, things like you can look at the tumor necrosis interleukin-6 factor alpha and IL-1 beta and things like that, and IL-6 and things. But those are not necessary typically. So we want to know if there's inflammation. Second thing we want to know is if you have insulin resistance. So many of us, and especially those of us who eat a Western diet, have insulin resistance. And that's really a double whammy. It gives you both a pro-inflammatory component because you have this non-enzymatic glycation that occurs. Of course, we measure it as hemoglobin A1C, but there are hundreds and hundreds of proteins that are glycated by these chronically high levels of glucose, also associated with fructose intake and things like that. It also, on the other hand, gives you the insulin resistance such that when you have insulin signaling, your body does not listen to it as well. It doesn't listen to it metabolically, and it doesn't listen to it trophically. So again, when we used to grow in a Petri dish, we would grow neurons for many years. You always have to include insulin in there because the insulin supports the survival of the neurons. So no surprise, when you start to reduce your insulin signaling, you're reducing the support for this tremendous neural network. You have about 500 trillion synapses in your brain. So it's an amazing neural network. And what's happening is you're literally downsizing that because you're not able to support it. Over time. So we want to know your HOMA-IR, we want to know your hemoglobin A1C, we want to know your fasting insulin and your fasting glucose. And then we want to know all the things that are trophic nutrients. So the 3 big things that support your brain, the trophic factors, the nutrients, and the hormones. So we'd like to know your estradiol level and your testosterone level and your pregnenolone level and your progesterone and your thyroid. These are all important, and cortisol is another one. So again, we'd We'd like to know, are you getting enough support? And then we'd like to know, what about nutritional support? Are you getting appropriate B12 levels, vitamin D levels? As we're learning, so many people who did not know that they were low in vitamin D until they got COVID-19 and suddenly were dying of COVID-19 or were having a really horrible course because of this association with low vitamin D levels, and that's been shown and published repeatedly. So if you think about it, Alzheimer's disease is somewhat like what's happened to various countries with COVID-19. So what happened with COVID-19? We have a pathogen, we have an insult, which in this case is SARS-CoV-2, and what happens? We're told, okay, you have to social distance, you have to shelter in place, you have to pull back. So we are pulling back from our interactions. We're not growing, we're not growing the economy, things like that. So we end up in a recession, we're pulling back, and this is very much like what's happening in an Alzheimer's brain. You have the combination of insults and poor overall support. And so your brain is saying, okay, I have to go from growth mode to protection mode. And guess what? When you make that amyloid, you make the stuff that we associate with the Alzheimer's brain that has an antimicrobial effect, as was shown by Rudy Tanzi and Robert Moyer from Harvard a number of years ago. This is a protective substance, but part of the protection is telling you we're going from growth mode to protection mode. So you're going to be protected from these various pathogens, but in so doing, you are now downsizing the network. So until you determine what is causing that downsizing and reverse that problem, you're going to continue to downsize. You're gonna continue to smaller and smaller neural network. So then we wanna know your vascular parameters as well. Mm-hmm. Because again, many people have problems. So it is a whole area of energetics you need not only the trophic support for your brain, the hormones, the nutritional, the nerve growth factor and BDNF, but you also need the energetics, which means blood flow, which means oxygenation. So many people are putting themselves at risk because they have poor nocturnal oxygenation. So they're not getting the support that they need. In fact, there's a wonderful paper showing just taking the average oxygenation, oxygen saturation at night, you can map that onto the the size of various nuclei within your brain. So as your oxygenation goes down, whether from sleep apnea or upper airway resistance syndrome or other things, the size of your brain starts to decline. And again, most people aren't checking. Most people don't know it. It's just like we all know our cholesterol. We should know our nocturnal oxygen saturation. We should know our hemoglobin A1C. We should know our fasting insulin, our HOMA-IR. We should know our HSCRP. These are critical. And of course, the The good news is there's a tremendous amount that we can all do now with quantified self, which wasn't available 5 or 10 years ago. Now you can get an Apple Watch, you can get an Oura ring, you can get a Bedr, you can get so many of these things. You can check your blood pressure, your microbiome, your insulin status. You can check your— there's CGM now, continuous glucose monitoring, which your doctor can write for you. So you can actually do all these things. You can, you know, you can check your your oxygen saturation all night long with an Apple Watch or things like that. The Oura Ring can tell you if you have a little bump in temperature. And by the way, a number of people have found out very early on that they were getting COVID-19 because of their Oura Ring.

Really?

Yeah.

I wear one myself.

Good idea. So yeah, you get a little bump, check and see what's going on there. So there's so much that we can all do that we couldn't do before. It really is leading us into a new era in which chronic illness will be much less common. You know, what's happened to us is We are all now dying of complex chronic illnesses. 100 years ago, most of us were dying of simple illnesses, TB, diphtheria, things like polio, things like that. Now we're virtually all dying of complex chronic illnesses, and these can be prevented. The good news about them is that you can see them coming if you know what to look for. The bad news is that they don't give you symptoms until they're mostly over. So that's just like with Alzheimer's. You're getting this long play out. Out before you get a diagnosis. So we need to be looking earlier and earlier, and larger data sets. There's going to be much more in the computational world that will help us with larger data sets, with looking at this complex machinery. We've had this unbelievable complexity gap in medicine where we look at very few parameters for people, and then we tell them, we don't know what causes Alzheimer's disease, and there's nothing you can do about it. We'll give you a drug that doesn't work very well. And you're going to die. I mean, that is barbaric. We will look back on this period as the dark ages in these complex chronic illnesses.

Well, you've touched on so many incredible points there, and potentially for someone who is not very deep into medical knowledge and testing and very reliant on, let's say, their local doctor who mightn't have this training, can you talk a bit about how you and through Apollo Health have actually prepared everything and the service that you offer to make it as simple as possible to get the right tests in order to track where you are and either pre-code, right? So one of your protocols to prevent it or to reverse it if you're already on that decline path.

That is a great point. So the major goal here is to reduce the global burden of cognitive decline and ultimately the global burden of neurodegeneration. We're starting to take the same sort of approach and adapt it to the unique biochemistry of each of the other neurodegenerative diseases. For Lewy body, it's different for Parkinson's, it's different for frontotemporal dementia, it's different for macular degeneration. We're just starting to look at these others. But the idea here was let's now train physicians. And so we've now trained over 1,700 different physicians in 10 different countries and all over the United States so that people can go to people who have been trained in this area. Having said that, of course, It's continuing to evolve. We're continuing to understand because again, the human brain is complicated. So we're continuing to understand, okay, what are the critical things? And a good example is a few years ago, we didn't recognize plasmalogens as being one of the important players, and some brilliant work from a biochemist, Dr. Dayan Goodnow, who has looked at plasmalogen, and these things are dramatically reduced in Alzheimer's disease. So ongoing work from his group. We'll see how important this is. You know, again, it's just What's the outcome at the end of the day? How much better can we make people? How much can we prevent this? Now, as you indicated, we then broke this up into reversal and prevention. In the long run, of course, we'd like to have everyone on prevention. And so we suggest that anyone, just like we all know that when we turn 50, we should get a colonoscopy. And actually my wife and I had his and hers colonoscopies on Valentine's Day.

How romantic.

Yes. Let's get this over with and let's just put this behind us. It's not a particularly pleasant thing to do. Now, interestingly, cognoscopy is much easier. So we recommend, look, anyone who's 45 or over should get a cognoscopy. Why? Because this problem, the cognitive decline that we used to think of as a problem, a disease of our 60s, 70s, and 80s, is really a disease of really late 30s, 40s, 50s, and it's just that you get the diagnosis 20 years later. So everyone everyone has had that feeling. Wow, you know, I'm in my 40s. I'm not as good at staying up all night as I used to be. I'm not as good at organizing things. I don't have the memory I did in my 20s. Okay, that's an issue. And so we're told, oh, you're just getting a little older. No, what this means is your metabolism is changing. You may have a little bit of insulin resistance. You may have some ongoing inflammation, as they say, inflammaging. It's a critical part of the aging process. There is a reason for being less sharp than you used to be, and in fact, performance is critical. And so, what we do is get a cognoscopy, and you could actually go online and get this directly, MyCognoscopy, if you want to, or go to your doctor and talk about this. But you want to know 3 things. Number 1, you want to know a set of blood tests, and some of the ones we've just talked about are in there. Number 2, you want to know an online cognitive assessment. It's pretty It's simple. You don't have to spend hours and hours with pencil and paper to get a cognitive assessment anymore. You can do this in 20 or 30 minutes online. And then the third part is optional, which is an MRI with volumetrics. That's optional. If you're asymptomatic, you don't need an MRI. If you're having symptoms, you should then get— if you're clearly having some cognitive decline, please get one. So we recommend, again, everyone 45 years or older. Now, if you're asymptomatic, we developed what's called PreCode, which is prevention of cognitive decline. If you're symptomatic, then you want ReCode, which is reversal of cognitive decline. Because no surprise, once you've started down the pathway, you want to do more. And again, as a scientist, the idea here was we wanted to pull out all the stops. This is a terminal illness. If you have cognitive decline, if you are developing Alzheimer's, it's a terminal illness. Either we're going to make you better, or you're going to die. So this is a huge issue, and this is why, yes, you want to have extensive tests. Some people say, well, you know, why do I want to have all these tests? In some places, people will have to pay somewhere around $1,000 for these tests. Okay, but the average cost in the US for someone with Alzheimer's by the time you die is $350,000. It's because a lot of it's because of nursing homes. So actually, let's avoid that. Let's keep you out of nursing homes. Let's make sure that you do very well. And it actually makes a lot of sense, not only financially, but also for your cognition and for your family members. So that's the idea. And actually, pre-code was a couple hundred dollars because you need fewer tests. There's less you need to do. But the idea is, whatever you're going to do, please get on top of it. Some people will think that, hey, I'm doing pretty well, but I want to check. We had one woman who came in, for example, who said, this is common in my family, Alzheimer's. She turned out to be ApoE4 positive, and she said, I think I'm okay, but I just want to make sure. She was in her late 40s. She took a simple test called the MoCA test, which is for Montreal Cognitive Assessment. It goes from 0 to 30, and most people should score 28, 29, or 30. Even 28's getting a little suspicious. She scored a 23. So she had very significant MCI already, mild cognitive impairment. She was on her way to Alzheimer's. Now she may not have had full-blown Alzheimer's Alzheimer's for another 10 or 15 years, but she was clearly on her way. She went on program, she's now at 30 doing very, very well. And so again, get in early. This idea that, oh, don't worry about it, it's just a little bit of aging. What happens is doctors, because they have nothing to offer, tell people year after year after year, yeah, it's mild, it's just aging. And then finally one year they say, oh yeah, this is Alzheimer's, there's nothing we can do for you. We'll give you a drug that doesn't work very well. It's barbaric. Brick. This is a paradigm shift out of the dark ages to making it so that there should be— this should be a rare condition. Alzheimer's disease should be a rare disease instead of the incredibly common disease that it is today. What the research showed us is Alzheimer's disease at its heart is an insufficiency. Now, it's a complex insufficiency. It has to do with all the things we talked about. But nonetheless, it is an insufficiency, a little different than scurvy, vitamin C insufficiency, or the rickets you would get from vitamin D insufficiency, but it's the same idea. It's an insufficiency of a complex neural network, a plasticity network, essentially. And if you continue that insufficiency, you just continue to downsize.

Thank you for that explanation. And I think it's so revolutionary that there is actually a solution. And I think it's just this general acceptance still feel, and this is part of the point of having this conversation, that if you're on that path, there's nothing you can do. Why is it that this isn't more widely known? I mean, in medical schools, there's not obviously much information around nutrition. And as you called it in your book, you know, Alzheimer's is a 21st century disease. So it's this paradigm shift of actually having to look at the multifaceted causes and not just focusing on, on one aspect. Where do you think the biggest challenge is in getting out this solution to solving Alzheimer's.

You know, this is a great point, and I wrote about this actually in a book that's coming out in August that's called The First Survivors of Alzheimer's. And we have some wonderful stories. This is from 7 different people who wrote their own first-person stories about what it was like to be told that you have Alzheimer's disease and then to get better, to be told that you're going to die and then to turn around. And so we had one woman as an example who is actually a nurse professor herself, herself, a nursing school professor, and developed the problem. She had a strikingly positive amyloid PET scan. She went actually in for a drug trial, and she was put on a drug. With each time she would get the drug, she would actually get much worse, which is something we've seen a number of times. These are drugs that are attempting to remove the amyloid from your brain. But again, no surprise, this amyloid is there because there's an ongoing insult. So you're now trying to remove the protection. So each time she would get this, she would get worse. So she then, after several of these injections, said, you know, I've got to quit this trial. She then ended up starting on the protocol that we developed, and she's now come also back to a perfect 30 with her MoCA scores. She's done very, very well, and she's sustained that. That's the most important thing is when you improve, you sustain the improvement because you're getting at the heart of what's actually causing this. But here's the problem. What started out with medicine, with academics, with neuroscience became what? Politics. It became pharmaceuticals. It became a huge industry. Drugs for Alzheimer's sell multiple billions of dollars per year to do virtually nothing. As you probably know, there's an ongoing issue right now. One particular one, which is called aducanumab, had a trial that failed, had another trial where it didn't improve people and it didn't stabilize, but it seemed to slow the decline a bit, and it did reach statistical significance at one dose in one trial. The FDA denied that drug, they turned it down for approval. And so then a statistician within the company reevaluated, in quotes, the data and said, oh, oh yes, it did, it did work. We're going to go back to the FDA. So went back to the FDA. The FDA then brought in a panel of experts that said they strongly recommended this should not be approved. There is not enough evidence to suggest that this has a positive effect. Despite all of that, the FDA is still considering it and will render its decision in June 2021. So upcoming June, and I won't be surprised if it is approved. There, in fact, the Alzheimer's Association is lobbying to approve it, even though it doesn't work. And so it's, as I said in the book, it's a little bit like saying to someone, I know this parachute doesn't work, but I'd like to wear it on the way down, and I'm willing to pay $100 billion for it, which is what, again, any drug that works well for Alzheimer's will be a $100 billion drug ultimately. Over the years. So we're unfortunately in a situation where in politics, the least important thing is truth. It's all about perception. It's all about support you can garner. It's influence, it's bullying, it's anything but the truth, which is again, one of the least potent weapons when it's coming to things like politics and finances. And unfortunately, that's where we are. And sadly, people are dying because of of this, and we can do much, much better. And so when we say, even though we've published repeatedly 100 people who improved a couple of years ago with 15 different clinics, and yet there's this requirement, an expert will say, it doesn't work until we bless it, until I say it works because I'm the expert. So we're in a very interesting situation right now. And as you know, there is a schism in medicine. When I was training way back in the 1970s, '70s, we all kind of agreed there was a very clear definition. You know, you're going to do this, you're going to— you come in, and medicine in the 20th century was about what? What is it? We learned to make a diagnosis. Is it Alzheimer's? Is it Parkinson's? Is it Lewy body? Is it diabetes? You know what it is. You made a diagnosis, and then either you write a prescription or you send them to the operating suite. So you're going to have surgery, you're going to have medicine. Now, 21st century medicine is completely different. It is about why it is. So it's not good enough to say this is Alzheimer's. Saying someone has Alzheimer's is like in the 1600s when we would say people had fever. They died of fever. Well, wait a minute, fever due to what? Later we figured out, okay, fever due to tuberculosis, due to pneumococcal pneumonia. It's just as silly to say that someone died of Alzheimer's because it means nothing. Alzheimer's is a person's name. It just means a pathology of plaques and tangles and neurodegeneration in your And so this is like taking your car in, you know, you take them to a mechanic and you say, my car's not working very well. And the mechanic says, oh, Claudia, we know what this is. This is car not working syndrome. You're like, what? And you, you know, and so that's what you say.

I wouldn't pay for that servicing.

Exactly. And so you say, look, your car is not going to do well. And you say, well, hey, aren't you going to check to see why the car is not working? Don't you want to know what's going on with the gas, with the oil, with the transmission fluid? Fluid, with the gears, all that. Like, no, we don't do those tests because they're not reimbursed. And that's where we stand with Alzheimer's. It's so backward because we've looked at this idea that we're just going to treat the pathology instead of to understand. So there is a schism in medicine, as I said, the phenomenon of precision medicine approaches, of integrative medicine, of functional medicine, of understanding why is considered to be wacky or crazy or alternative. But the surprise is, and I wasn't trained in that kind of medicine, we have just brought this directly from the test tube. So 30 years of research in the lab and looking at, okay, what are the things that actually drive the problem? Then you can see that there are these multiple different things. You can literally trace the molecular species, estradiol as an example, binds to its estrogen receptor, enters the nucleus, it affects the transcription, the production from DNA of RNA species of hundreds of different genes. And one of those genes is the one that's on the synaptoblastic side, something called alpha secretase that causes your APP, your signaling molecule, to go onto the synaptoblastic side. So you can literally trace the pathways of all these various molecules as they put you on the good side or the bad side. Mm-hmm. And so, look, I didn't wanna think about integrative medicine or functional medicine. I thought all that stuff was woo-woo, was silly, you know, but as a scientist, the science actually supports that kind of medicine. Yes. Not the kind of medicine that I was trained in in the 1970s and 1980s. So, okay, I can't deny the truth. I can't deny the outcome. Even things that address problems like stress. You know, I thought this was all silly, like you're going to address stress meditation. Look, just take the right drug, you're going to be fine. No, that's not actually the way the human body works. So let's quit denying the truth. Let's look at what actually causes cognitive decline and let's address the things that cause that. And we can already see, and we've published repeatedly, you get much better results by doing that. And by the way, the pharmaceuticals will be very important. But they shouldn't be used as monotherapies. Think about it. The way we're being treated now is it's a monotherapy, it's monophasic, it's going to be the same thing forever. What? It's uniform, the same for each person. Really? There aren't different causes? And it doesn't address what actually causes the decline. So it's like taking 100 cars that are all not working well and filling each one up with gas and saying, let's see if that Well, it might work for 2 of them, but it's not going to work for all 100. Let's figure out what's causing it. So when you are going to treat optimally, you want to look at all the different things and you want to address all of them. And it might take multiple phases and you might want to change. We find that, you know, tweaking things over time is critical. As an example, we had a woman who did quite well on the first set of things, but then after a couple years she was saying, you know, something's not quite right. I'm starting I said, okay, well, we need to look at what's a problem now. And she resisted that at first and said, well, look, I've already been evaluated. How much more can we find? Well, it turned out interestingly that she had an undiagnosed tick-borne infection, which is called Babesia. You get it when you get Lyme disease. It's a co-infection. She had been treated for Lyme years ago and had never had any problems with that, but she hadn't recognized, and by the way, over 50% of people who get Lyme disease have one of the co-infections, Babesia or Ehrlichia or Bartonella or others. And she turned out to have Babesia. So when her Babesia was treated, she once again improved and she's done very well. And by the way, she's also, she turns out to be a 4/4 as well. So very high risk for Alzheimer's and was in the earliest stages, but now doing very, very well. So it's not always a monophasic, you continue to tweak. Again, this idea, we physicians have gotten away over the millennia with very simple approaches to treatments. If you think about it, if you have pneumococcal pneumonia, your likelihood of getting pneumonia has to do with a lot of things. If you have alcohol on board, you increase your risk. If you have Type 2 diabetes, you increase your risk. If you have problems with your B cells, so for example, people who If you have multiple myeloma, have increased problem with getting pneumonia. If you have a poor immune system, all those things. But because the pneumococcus itself is far and away the most important player here, we have gotten away with simply writing a prescription for penicillin or ampicillin or other things like this. However, complex chronic illnesses don't work that way. When you get Alzheimer's, there are dozens and dozens of different potential contributors. We initially identified 36. There are a few more. The good news is it's not thousands, it's dozens. So you have to look, but not a single one of those is like the pneumococcus. If you just treat that, everything else goes away. So that is the problem, that this is fundamentally a different type of illness. And so people have argued about how to treat it. And a great example is COVID-19. COVID-19 is a simple illness. As problematic as it is, it's still a single virus. We know how to treat a virus. We want an improved immune system. We want to have a vaccine. We want to have antivirals. All these things have been developed. It's fantastic. And people are continuing to develop better and better antivirals, things like that. Now, of course, the big problem now is that we're having to deal with mutants. And interestingly, there's one group that's actually developing antivirals that the mutants can't get around, which is very exciting. But at the end of the day, it's still a simple viral illness. On the other hand, there's a big argument about what Alzheimer's is. People spend their whole careers working on the notion that Alzheimer's disease is due to, quote, misfolded proteins. Others say it's reactive oxygen, it's metal binding, it's an infectious disease, it's type 1 diabetes, type 3 diabetes. It's a prion. There's no agreement on what this actually is. So our point is that what the science tells us this is, is a signaling imbalance in this beautiful plasticity network. And of course infections are part, but not just one infection. You can trace many different ones. There can be herpes simplex related. It can be P. gingivalis, which is a change in your oral microbiome. It's associated with poor dentition. It can be many other organisms that have been identified. Chlamydia is another one that's been associated with cognitive changes, HHV-6A. So when you look at the epidemiology of Alzheimer's, it's bewildering. There's all these different things and you say, well, how can that be one disease? Well, that's the point. It is an alteration in this balance. So you have to look at all these different players and you have to address the ones that are causing the problem, not just write a single prescription for one thing and, as we've seen, get no improvement. So this is not a monotherapy disease, but the drugs should work better on the backbone of an optimal protocol.

Thank you for that explanation. And I think addressing the causes is relatively new for Western medicine by really looking what's behind it. But if you look at Eastern medicine, this is what they do. I mean, I think a perfect example For example, I, in Shanghai once, in China, visited a traditional Chinese medicine pharmacy, and then the diagnosis upstairs, which was interesting. They look at your tongue and check your pulse, and it's a bit different. But she was really explaining that in Eastern medicine, if you have a headache, they need to find out why, and you're treated for that why. And you might have a headache for 3 days, but they will cure you of that headache coming back because the cause has actually been solved, which is so different to Western medicine. You have a headache, I take a comes back again tomorrow, take another pill, and all of a sudden you're taking all these pills on a daily basis instead of actually looking at the root cause. So there really needs to be a paradigm shift in the way that medicine is looked at and not just solving for the superficial, but actually going down to the cause. Are you seeing more and more researchers focusing on that?

Not yet, although yes, a number have. But this, again, this is not yet considered the norm when of course it should be the standard.

Standard.

And the response is, you know, this is not the way we were trained, this is not the way this works. So it's interesting to me there's been so much pushback. There is a lot of resistance to progress, to looking at new things. And, you know, you indicated Eastern medicine, and the reality is we now need to train physicians that have the best of both worlds. So the traditional Eastern physicians did not know anything about RNA or DNA or molecular biology or large data sets and all that. They were looking at the whole organism, as you indicated, but they didn't look at these various molecular pathways. The traditional Western physician would understand DNA and RNA and things like that, but would focus on one thing. They would say, aha, it's misfolded proteins, we're going to give you a prescription for something that doesn't work. But the reality is we now need to train a new type of physician that combines those to that looks at larger datasets. You know, it's so interesting to me that we've used these very complex algorithms to figure out where Claudia shops. So, Google knows where you shop. Google knows a lot about you, as they say, probably more than you want them to know.

Exactly.

Exactly. Why are we not using the same sort of complex algorithms to make people better? So, we're really great at knowing where they shop. Shop, but we're allowing them to die of Alzheimer's. Again, this is barbaric. And, you know, this will— this will— we'll be laughing at this in 10 or 20 years and saying, oh wow, we were so backward. And of course, part of the answer is because people go where the money is. It's very lucrative to know where you shop, and it hasn't been so lucrative so far to prevent people from getting Alzheimer's disease. But this is the way we need to go.

The lobby of the pharmaceutical industry is obviously very, very strong, and there's billions to be made for prescribing. So I think that that's the conflict of interest that is happening there. You touched on the Precode and Recode, and I think for a lot of people that mightn't have a physician, is it possible to access from anywhere in the world these protocols that you have in place that are prepared on the Apollo Health website? And what if there was a physician that they trust but would like to get trained in this? Could you walk through the process how someone could approach this?

Absolutely. And you can start online very simply, like everything else. And there is, by the way, a lot of telemedicine ongoing because of the pandemic, of course. And so many people don't have to do the traveling that they used to, or they could travel one time and then not have to go back for quite a period of time. And so, yes, you can look at drbredesen.com, you can look at mycognoscopy.com to look to see how to get this. You can look up Precode or Recode or ApolloHealthCo.com. So many ways to do this. And there are people trained all over the world, in Japan and in Australia and in the UK and in the EU. For example, there's a wonderful group in Edinburgh led by Dr. Charmaine Shepherd and Dr. Jean Dow, and certainly talk to them. And there are the people all over the UK And I'm sure you know Dr. Rangan Chatterjee, who's a wonderful doctor who's been on television numerous times, does a great job, and is very up to date on functional medicine. And he was actually one of the first students who came to our course on cognitive decline at the Buck Institute years ago. So Rangan is very familiar with the sort of thing that we're doing. And of course, he's had quite good success. With things like type 2 diabetes and obesity and all these sorts of things based on practicing of functional medicine. So there are numerous people around— Dr. Michael Ash, another tremendous practitioner in the UK. So there are many people who are doing the new kind of medicine. And again, when it comes to chronic illnesses, you know, this should be called effective medicine. Some people have called this sort of thing alternative medicine, and I, I would say you should call it effective medicine because when it comes to complex chronic illnesses, standard of care medicine does not help.

Yeah. And fantastic that your model also trains medical practitioners and also nutritionists, I believe, in this. And how long does that training take in case there are some listeners who are doctors interested in this?

Yeah. And it's now available online and it's about 35 hours right now. And we're also continuing to enhance it and update it all the time. We've had, again, a number of people who've taken the recent course, which is Recode 2.0.. And so again, that's about 35 hours. And we have some tremendous experts, Dr. Neil Nathan, who's a world expert in mycotoxin-related and biotoxin-related illness. And this has turned out to be, you know, again, I, when I was trained, never was taught anything about, hey, biotoxins are important in illness. But it's, again, I can't deny it. It turns out that when we look at people, what's actually driving the problem. It's a relatively common contributor that people have biotoxins, just as other people have inorganic things like metallo-toxins or air pollution. There's a lot that's been written now about air pollution and its relation to cognitive decline. So those of us here in California who were unfortunately in the California fires are now at increased risk for cognitive decline and have to be very careful. The people who were in the World Trade Center cloud, there was a paper shown in— by 2016, 13% of those people had cognitive decline. So because this tremendously increased exposure to various toxins and then organic toxins, things like glyphosate and benzene and toluene, there is a burst of Parkinson's disease. It's, by the way, of all the neurodegenerative conditions, conditions, it is the one that's on the most rapid increase. And that has been linked to exposure to these various organic toxins, things like trichloroethylene and perchloroethylene, things like that. So, and Paraquat and on and on. So again, it's important to know whether you have exposure to these things. So many of us have a toxic burden that we deal with throughout our lives, but no one's checking for it and we're not doing anything about it until we end end up having a disease, whether it's Parkinson's, whether it's Alzheimer's, whether it's ALS, another important disease that is toxicity related. So this is a major problem. And so you can be trained in this by checking, and again, there's about 35 hours or so, and we're continuing to add additional physicians. I mentioned Dr. Neil Nathan, also Dr. Chris Shade, who is an expert in chemotoxicity, also Dr. Cyrus Raji, who's an expert in imaging. Dr. Anne Hathaway, who's an expert in bioidentical hormone replacement, which again, turns out to be very important to get optimal cognition for, you know, the right age group and used in the right way. All of these things are critical for best outcomes.

And it just really shows how important it is that each individual is on top of their health, is aware of the tests that they should take, particularly if they have a family history of Alzheimer's or cognitive decline. And it is possible to then stop it. I'd love to take a step back and perhaps you can tell listeners where this journey to finding the protocol actually began. Have you always been fascinated with neurodegenerative diseases? How did you stumble, if you will, on this path?

Yes, I was a freshman at the California Institute of Technology and I read a book about the brain called The Machinery of the Brain. The Brain by Dean Wooldridge of TRW fame. And he talked about the relationship between computers and the brain. And I was interested in computers and I thought, oh, this is really interesting. You've got this amazing computer inside your skull with a huge number of synapses. And I started reading, got very, very interested in what the brain was all about and how it worked. And ultimately I got interested in why we have diseases of the brain and why they're such horrible diseases. You know, if you look looking at the various types of disease, the area of greatest biomedical therapeutic failure has been in the area of neurodegeneration. So, you know, again, as someone said, everyone knows a cancer survivor, no one knows an Alzheimer's survivor. And of course, you could say the same thing for ALS and frontotemporal dementia. So now we know of many survivors, but we didn't know back then. So that's when I decided— I actually worked at MIT and Caltech, and then I decided to go medical school to learn about the diseases of the brain. And the idea then, when we started the lab, and I was very fortunate to train with Dr. Stan Prusiner, who won the Nobel Prize in 1997 for his discovery of prions, which are critical in neurodegeneration. And so we wanted to understand, could we develop simple models, much as the oncologists have developed simple models to study cancer in a dish, so that they can look at the molecular detail and look at things like oncogenes and tumor suppressor genes. And by the way, they came to the conclusion that there was an imbalance in a signaling pathway that has to do in this case with growth and survival. You've got turnover of cells, so you've got oncogenes that are driving your cells to divide. You've got tumor suppressor genes that are causing your cells to commit suicide. And for most of your life, you have this beautiful balance that allows you to shape your organs and allows you to develop your brain and all these wonderful things and heal yourself yourself. But of course, if you do things wrong, you smoke too many cigarettes, or you get exposed to chemical carcinogens, there's a chance that you will change that balance either by increasing the activity of your oncogenes or decreasing the activity of your tumor suppressor genes. Typically, it's some of both, and you then have this phenomenon, and it does have to do with metabolic state and things like that, and your immune status, because your immune system is quite good. And of course, now we, we treat this in part by enhancing the immune rejection of tumors so that you get this imbalance. And what we discovered in the lab and what we set up, then the same idea we set up so that you could have a simple system to study the neurodegenerative phenomenon. We first described, we described the first examples of neurodegeneration in a dish so that we could now discover the various genes and processes that were related to that process.. And we found the same thing, that there's an imbalance between, as I said earlier, the synaptoblastic and the synaptoclastic. So then you have to ask, okay, what's causing it? And the surprise was it's not a single gene. It's not just something where, oh, you know, I caught an organism, I caught—

that would be too easy.

Yeah. It's just, it is a complex chronic illness. Now, you know, maybe someday we'll know that there's something really simple and we can give a single drug and it will do everything. Everything. But I often show a slide to people that says, here's what the drug would have to do. And, you know, there are 100 different things. There are all these things. It would have to make you more insulin sensitive, and it would have to make you have an optimal thyroid, and all these things. It would have to heal your leaky gut. It would have to get rid of your HSV. That's a lot to ask of a drug. So I think that the drugs are going to be great as part of an overall program, but you want to get at what's actually causing. So all these people who've been trying to reduce your amyloid, that's getting at one of the mediators. Absolutely, that's a mediator, but it's not the cause. Yeah, that's the difference. And so we got to be very careful about the semantics. What is the cause? What are the contributors? And what is a mediator of this problem? And in that system, we see these prions, which is, you know, these remarkable things which can cause this phenomenon that is like an infectious illness. These really are about amplifying a signal. So you have essentially two different kinds of signaling in your body. We talk about homeostasis. You know, your serum pH should be 7.4. You never want it to be too acid or too base. You never want it to be 2.4 or 10.4. So if you drink something, for example, that's slightly acidic, say like a soft drink, drink, then you want to return your pH to 7.4, and you use both respiratory and metabolic compensation to do that. That's negative feedback. That's homeostatic feedback. On the other hand, when you desire a multi-goal outcome that requires amplification, and a good example is blood clotting. If you're a caveman and you cut off your finger, you're going to die if you don't clot So you use a system that is feed-forward, and this is literally prionic loop feedback. You're taking a system that amplifies itself, and we believe that that's what prions are all about. So they are very important in things like memory, in things like plasticity. But unfortunately, when they run amok, they continue to pull back, you are going to have a degenerated brain.. And so again, we want to go upstream and say, why is this happening? What are the root, as you said, root cause contributors?

How long has the protocol been in existence? And can you talk about some of the success stories that you've had?

Absolutely. So what happened was back in 2011, we were screening for drugs that would change. We knew a little, we didn't understand the whole picture yet, and we're still learning more and more, of course. But at the time, we understood that there was a balance there and that we wanted to drive the signaling toward what happens with APP. APP is the amyloid precursor protein, which is at the center of this. And when things are good, your brain senses this. It senses your status with your trophic factors and your hormones and your nutrients and your inflammation, all these these things. And it says, things are good, I'm going to be cut at a single site and produce two peptides, one for outside the cell, one for inside the cell, that say growth and support. And this is no different than what happens in your country. Look at the difference between what your prime minister has been doing when things are good versus when things are bad. Okay, he's been wonderful about saying, we've gotta be careful, we've gotta get the vaccine, we gotta do the right thing. Okay, now we're ready for growth mode, and you're either in one mode or another mode. Your brain does the same thing. And so when things are good, you make these two peptides, SAPP alpha and alpha-CTF, which supports making and keeping synapses. On the other hand, when things are bad, you make four fragments. And so you now are going to tell you things, okay, we're going to pull back and we're going to go into protection mode. And so then we screened for drugs back in 2009, 2010, and by 2011, we actually had some wonderful drug candidates. And so we actually applied to do a clinical trial, but I was sitting in my office looking at the whiteboard, and I thought, well, wait a minute, you know, this is not addressing many of the things that could actually be— so our drugs could fail, our drug candidates, So I thought, well, wait a minute. I knew that one of my colleagues, Professor Mike Merzenich, who developed, who came up with brain training, brilliant guy. And I thought, well, what if we combined— he's doing these studies on brain training, which again were helpful for some people but not all. And I thought, what if we combine that with the drug? Could that give us a leg up? I thought, could that maybe help this drug to work better? And then I thought, well, wait a minute, It kind of— the light bulb went off, and I said, why would we deny people any of the things? Why would we say, let's just take one? And that kind of went, oh, wait a minute. Okay. So we then applied to do the first comprehensive trial. That was 2011. And the trial was to be done in Australia because the specific drug was available in Australia for other purposes. And we thought, okay. Okay, we're going to have a group that does placebo, of course, a group that does the drug, but then we're going to have a group that does all these other things that address the problems, and then a group that does all these other things with the drug. And of course, I was hoping that the drug with all these other things would really give us a big bang. Well, guess what? We got turned down by the IRB. The group that reviews this says, we're not going to allow you to do this trial because it's a multivariable trial. You're asking to test more than one thing. And we said, but wait a minute, this is a multivariable disease. So this is another one of the problems. The classical approach in medicine is to test only one thing. Well, you're outta luck then when it comes to a multivariable disease. So we've got to be better at looking at these multivariables. What we need to do is get something that works with multivariables and then, okay, you wanna take one away, Or the other way to go now with artificial intelligence, which is of course the future, is to look at large, large numbers of people who did all sorts of combinations and then ferret out, okay, this is the beginning. But again, people think if you're going to use a combination, you want to test each thing one at a time, and if that doesn't work, don't include it in the combination, which is silly. This is not a linear system. It doesn't work that simply. So you need to look at combinations combinations, and you can't expect that they're going to act the way of each thing separately. You really need to get over a threshold, which is just what happens, by the way, with cardiovascular disease. You have a threshold, as Dean Ornish showed years ago. You need to get over a threshold. So 2011, we got turned down. So we thought, oh my gosh, what are we going to do? There was a philanthropist that had supported some of the work. He got very angry at me and said, you know, what's wrong with you? You couldn't get this this thing approved in Australia. If you work for me, he said, I would fire you. And so I was very depressed in 2012. I thought, you know, how are we going to get this out there? I got a call from a woman who herself had just been diagnosed with Alzheimer's disease. She had called her friend to say that she was going to commit suicide. This is a woman who worked on the East Coast, 3,000 miles away from us, but her friend said had heard about some of our research and said, "You've gotta come to California and you've gotta see what these guys are doing." So I got a call from this woman, from the friend actually, who said, "Would you be willing to see my friend?" And I said, "Look, I haven't seen a patient in 20 years. I work on transgenic mice. I work on dying cells in petri dishes." I said, "I can tell her what we were going to do for this trial. That's the best I can do. And I can send her back to her own doctor." And so this woman came out and we spent 2.5 hours going through all this stuff. And she took all these copious notes 'cause she couldn't remember anything. Took him back to her doctor, and 3 months later I got a call. I thought I would never hear from her again. I got a call 3 months later at my home on a Saturday morning, and she said, I can't believe it, I'm back at work. I said, my memory is better than it's been in 20 years. Wow, great. So I hung up the phone and I turned to my wife and I said, this work— I was like, I was so excited. I said, I think we're on the right track. She actually came back then, and I— we did a little video and started talking about it as an anecdote. And then we assembled assembled many anecdotes with the idea being we need to go back to the IRB and saying, will you now allow us to do this appropriate comprehensive trial now that we have anecdotal evidence? So we published the anecdotal evidence and got all sorts of pushback. It's only anecdotal. Well, hey, you have to start somewhere if you're going to change things. So we then published 100 cases with documented improvement in cognitive scoring, in MRIs, in PET scans, et cetera, and in electrophysiology, so forth and so on. Then interestingly, we were turned down again for the trial in 2018. Then in 2019, they finally allowed us to do a proof of concept, which is the one we just finished. And now we're going back to do a larger study as well, because of course it's going to take some time to convince people. It's amazing. The history of medicine is replete with people being skeptical and being wrong. And so, you know, great example was Semmelweis, who believed in the germ theory at a time when very few people did. And he was roundly criticized. He was actually thrown into an insane asylum, sadly died from an infection himself because people didn't believe in infections. And if you look at the history of scurvy, people discovered a cure for scurvy each century, and then it would be turned down, and then they would discover it again. Rediscover it. So, you know, needlessly, hundreds of thousands of people died of scurvy because of this. And so now we're going back, 2019, we're going back and finish this. Now, it'll be a while before people will accept this, but meanwhile, we have wonderful examples again and again of people getting better. And things will change over time. As they say, the final piece is that people say, we knew this all along, this is nothing So we're getting there.

That's the day to really celebrate it. Very exciting news. Now, I wonder, would you say that the work that you have done, and because you get to the root cause, but could it be that this protocol that you recommend with ReCODE is not for everyone? Are there any exceptions?

So the trial that we just did, it took people with MoCA scores between 18 and above. That's significant. So usually it's said that, you know, 18 to 21 1 is Alzheimer's, and above that is going to be MCI, mild cognitive impairment. So the average for someone with full-on Alzheimer's is about 16.2. So this study did not include people who had MoCA scores of 0 or 2 or 3, that sort of thing. I'm interested now in setting up a separate test, which is going to be called the SARA, Severe Alzheimer's Reversal Attempt, for people from 0 to 7, We'll see how it goes. So the question is, what can we do for people who are farther along? And I'm interested in this specifically because we have had a number of people who had scores of zero who showed improvement, but they are the exception, not the rule. What are we missing? What do we need to have people who are farther along? So I think you could say that what we've just finished is MCI and early Alzheimer's. This is not yet for late-stage Alzheimer's, even though, yes, we have anecdotal success success for people with late stage, but you have to look, it's harder. You've gotta look and you've really gotta address all the things that are contributing to this change. This is no different than someone who's got late stage cancer versus early stage cancer. Sure. People have always said, of course, it's easier to deal with early stage cancer than late stage cancer. Yeah. And so we need to understand, are there additional things? Do we need to include stem cells? Do we need to include intranasal trophic factors. You know, what are the things that need to be added? As I say, we do have anecdotal improvements, but that's not the rule. So I would say that, ask everyone, if you don't get on prevention, please get in as early as possible for prevention. People will say, oh, you came in early, it's not Alzheimer's yet. Well, why would you want to wait for it to be Alzheimer's? Just like prediabetes, you know, again, they used to say you either had diabetes or not. Of course, now we We recognize before diabetes is prediabetes, before diabetes you often have some insulin resistance. So this is a spectrum. Why would you wait? You know, get started early. We need to change the classical thinking about this, the way we think about these illnesses. So I would say for the moment, there's nobody that it's not for because there are not alternatives, but no question, it's easier to do it if you're in the earliest stages.

Yeah, no, that makes sense. And you said for the clinical trials, are they all California-based? Or if there's people listening who have a loved one or family member that is maybe late stage as well, would you look for people around the world to also participate?

So we're getting there and there are other trials that are now starting. For example, Dr. Heather Sandison is doing her own trial that is in San Diego. So still Southern California. Yeah. The one that we just completed was in Northern California and Oregon. Oregon. I was really blessed to work with 3 fantastic physicians, Dr. Anne Hathaway, Dr. Kat Toops, and Dr. Deborah Gordon. Deborah is in Oregon, and all of them are very well trained. They're all fantastic integrative and functional medicine physicians and all getting just tremendous results with their patients.

Really fantastic. Can you talk more about the work that's to come with Apollo Health and also with the Buck Institute where you've been involved as well? Where do you see the next 3 to 5 years tapping out.

Yeah, so I had my lab at the Buck Institute for 20 years, and so now we are— we've gone from transgenic mice and cell culture and things like that to working with human patients. That is the future. And so what we're doing now is called the ARC Project. Noah's Ark was 2 by 2 by 2, and I really believe that in this day and age we can learn the most, especially in these impossible illnesses, these illnesses that have been so difficult to treat, things like ALS and things like macular degeneration and things like that, from having very large datasets on a few people. Instead of getting large numbers of people with tiny datasets, we want to have massive datasets on tiny numbers of people. That will begin to point us in the right direction. It's not an efficient use to do— to say, okay, we're going to take this huge number of people when we really don't know what we're doing. And as you know, billions of dollars have been spent on these clinical trials where you're really barking up the wrong tree. You really don't have a good understanding of what the disease is. This is not a simple virus. This is not a simple bacterium or spirochete or fungus. This is a complex problem. And so, you need to take small numbers of people. So, we've just started this. We've started working with the first few people with macular degeneration, actually. By the way, Lewy body patients turn out to respond quite well. They are very much like our type 3 toxic Alzheimer's disease. As you know, having Lewy body is a little bit like having some Alzheimer's and some Parkinson's. That's actually what the genetic studies recently have shown, the same thing. Genes associated with Alzheimer's and with Parkinson's are ones that are associated with Lewy body disease, including APOE, by the way, APOE4. The idea then, that's the way things are headed. We're looking at expanding datasets and looking at applying the same approach but with the understanding of the unique biochemistry of each of these diseases. Now, Apollo was created specifically to do software because we need complex algorithms. Again, this idea that we're gonna do medicine like it was done 100 years ago, and we're just gonna write a prescription, it just hasn't worked for these diseases. So we need to change the way we think about this. We do need to get people in earlier for prevention and early reversal. We need to collect larger data sets, and we need to have better and better and more and more sophisticated algorithms algorithms. Computers should be helpful to doctors. Yes, we've used them for things like electronic medical records, but they should be your assistant. Claudia, if I said, okay, here's your genome, there are 3.3 billion base pairs. Of course, you need help from the computer to tell you what are the critical SNPs for your, the critical mutations, et cetera, for your health for the future. Of course, you need that. And you're going to need that for best outcomes for all of these complex chronic illnesses. And so that's why we created Apollo Health.

Excellent. If you had a crystal ball, as we all would like to have, what would you say would be the medicine of the future? What would be the perfect lifespan health, well-being testing model?

What could you foresee coming in the future about how we can prevent diseases by knowing more earlier Yeah, and I think you're going to see tremendous changes, not only in complex chronic illness and of course in the closely related phenomenon of aging. I think that it will be very routine for people to age much better. And, you know, in the United States, we age very poorly. And in fact, there was a study done. I was on the National Aging Council years ago, and an excellent epidemiologist did a very interesting study showing that in the United States, in the United States, we get our first chronic illness, whether it be hypertension, type 2 diabetes, beginning cognitive changes, all these sorts of things. We get our first one on average in our 40s. Wow. It's horrific. And on the other hand, as he showed in the UK, you get your first complex chronic illness in your 50s. So in fact, your health is better. Health span is better in the UK. And having said that, the UK and the US both do fairly poorly on the world stage of longevity. If you're in France, you do better. If you're in Japan, you do better. If you're in Italy, you do better in terms of average longevity. So we have relatively short health spans. And this is one of the reasons that United States spends so much on sick care. Our healthcare health bill is a huge, huge bill. It's between 15 and 20% of our GDP. It's horrible. And because we're not doing the right thing. So to answer your question, for the future, it's gonna combine 3 fundamental things. Number 1, there will be much better algorithms, much better software for helping you to manage your health. What we're doing now for health is barbaric. It's basically, we're trying to sell you drugs. We have these healthcare places that are trying to make a lot of money. It's horrible. And so we'll do much better throughout the span of your life with larger data sets preventing these illnesses. The second thing is there will be much more quantified self. You know, just as we know our cholesterol today, you'll have a very good knowledge about where you stand, where you stand with your where you stand with all these various critical— are you sleeping well? How much stage 4 sleep did you have last night? How much REM sleep did you have last night? How is your elasticity of your vessels? You can know that today, and you should know that. What are your genetics? You know, people have said, don't find out your ApoE status because there's nothing you can do about it. That nothing could be further from the truth. There is a tremendous amount you can do about it, and everybody should know it. You'll know all these different pieces, and you'll have— your physician and health coach will have set up a plan for you that optimizes your likelihood of developing complex chronic illnesses. Alzheimer's will be rare. Basically, we got rid of the diseases of the 20th century, which were the simple ones with things like antibiotics and public health. We will get rid of all of these diseases of the 21st century This is everything from lupus to rheumatoid arthritis to schizophrenia to Lewy body to Alzheimer's to Parkinson's to ALS. These are all complex chronic illnesses. We can see them coming. You can look at the right things and you can now deal with the arsenal for these things is huge if you know what to do and how to use it. And then the third piece of this is global vaccination programs. And when I say vaccination, I'm using that very loosely. I'm not talking about an injection in your arm. Arm. A global public health program to render these diseases rare. So go into all these different countries and say, okay, we have a very simple way to look at these. And I wrote about in the book that came out recently, the one that you mentioned, The End of Alzheimer's Program, about the idea that for an Alzheimer's vaccine, it's a quite different type of vaccine. It's not an injection in your arm. It's a program. Program that looks at all the different pieces and essentially pre-code. It looks at these things and then makes sure that you don't get this. And if you think about it, this is like a pyramid. What we're going to do is take the large number of people at the bottom of the pyramid and get them on a very simple program for prevention. Now, some of those will fall through the cracks, right? So now you'll have something like 5 or 10% of people that will say, oh, wait a minute, I— despite those things, I'm beginning to symptoms. Okay. We'll then do the next level of testing. This is the way you make it efficient. Okay. They'll have additional testing. Aha. Now we'll see for most of those people, it's this gene or it's that thing or it's this infection that you had or you've got a lot of toxic exposure or you do poorly with toxins. Those people will mostly be helped then by the next program. Now, a small number of those people, and you just go on that way. So after a couple of increases, now there would be a tiny number of people that will actually have to be inpatients. Something really is wrong here. We need to do something very, very significant with you. That's the way to make it so that it's efficient and yet gets a global reduction. So our goal is a global reduction in the burden of dementia.

What a great goal. Thank you so much, Dr. Bredesen, for your time and for these insights, and it can't be soon enough that these possibilities for people to reverse cognitive decline, to go on the journey of prevention. And there's so many knock-on effects. The change in diet that you recommend with the KetoFlex has knock-on benefits for many things, including type 2 diabetes. It's all interlinked, which is why functional medicine is so helpful to look at the whole picture together. It's been a real pleasure. Thank you so much for coming on today.

Thank you so much, Claudia. I really appreciate it. Stay safe.

Stay well. Hi everyone, this is Claudia again. Before you take off, thank you so much for listening to the podcast today. I hope you learned as many valuable insights on living better for longevity as I did. I'd love you to join our Longevity Tribe. Subscribe so we can learn and grow together, as well as hear your feedback. So please subscribe to the podcast and leave a review to let me know what you thought. Thanks so much and take care.